Gingival hyperplasia and folic acid deficiency from anticonvulsive drug therapy A theoretical relationship

Vogel, Richard I.

doi:10.1016/0022-5193(77)90199-0

Cited by 28 publications

(22 citation statements)

References 47 publications

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“…Phenytoin is not only responsible for the initiation of gingival enlargement but also for the interference of folic acid absorption thereby leading to a significant decrease in the folate levels (Norris and Pratt, 1974, Mallek and Nakamato, 1981, Lewis et al, 1995) suggested to be one of the important promoters of phenytoin-induced gingival enlargement (Vogel, 1977), a hypothesis later corroborated by Backman et al, (1989). There have been studies that report clinical benefits of systemic and/or topical usage of folic acid in delaying the onset and reducing the incidence as well as severity of phenytoin-induced gingival enlargement.…”

Section: Discussionmentioning

confidence: 83%

“…[5,6] It has also been seen that phenytoin is not only responsible for the initiation of the enlargement of the gingival tissue but has also been noted to interfere with folic acid metabolism especially, absorption thereby leading to a significant decrease in the plasma as well as the tissue levels of folates. [7] Folates administered at pharmacological doses, on the contrary, though have been seen to lead to a substantial decrease in the incidence of gingival enlargement, [8] have been blamed for a significant decrease in the serum concentration of phenytoin severe enough to precipitate seizures. [9][10][11] The use of folates as an adjuvant to the antiepileptic therapy in the prevention of gingival enlargement, therefore, mandates further clinical and laboratory evaluation.…”

Section: Introductionmentioning

confidence: 99%

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Risk assessment of folic acid supplementation in phenytoin-treated epileptic patients: A pilot study

Nayyar

Khan

Subhas

et al. 2013

Int J Nutr Pharmacol Neurol Dis

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Background:There have been studies that report clinical benefits of the use of folic acid as an adjuvant to the antiepileptic therapy in the prevention of antiepileptic drug-induced gingival enlargement. However, studies conducted in the past have also reported precipitation of epileptic attacks in patients on folic acid adjuvant therapy due to fall in sera levels of phenytoin due to drug interactions. The study was planned to investigate the association of phenytoin-induced gingival enlargement and sera levels of folic acid in epileptic patients on phenytoin therapy. Subjects and Methods: A total of 25 patients aged between 18 and 50 years clinically diagnosed with epilepsy prior to the start of phenytoin therapy were included based on selection criteria and written informed consents were obtained. Assessment of serum folic acid levels and gingival enlargement was done prior to the start of and after 6 months of phenytoin therapy. The statistical analysis was done using t-test and the baseline serum folate levels and the serum folate levels obtained after 6 months of phenytoin therapy were correlated with the respective grades of gingival enlargement using Pearson's coefficient formula. Results: The results of the study confirmed a significant association between low serum folate levels with increasing severity as well as an early onset of phenytoin-induced gingival enlargement justifying the judicious use of folate supplementation to prevent this inadvertent side effect of phenytoin administration. Conclusions: The results of the study suggest a higher incidence of gingival enlargement in phenytoin-treated epileptic patients with a positive correlation with falling serum folic acid levels as the duration of the therapy increases.

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Section: Discussionmentioning

confidence: 83%

Section: Introductionmentioning

confidence: 99%

Risk assessment of folic acid supplementation in phenytoin-treated epileptic patients: A pilot study

Nayyar

Khan

Subhas

et al. 2013

Int J Nutr Pharmacol Neurol Dis

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“…Reynolds berichtete 1968 über Zusammenhänge zwischen Folatmangel und psychiatrischen Befunden bei behandelten Epileptikern, Ergebnisse, die von anderen Autoren nicht bestä-tigt werden konnten (Norris und Pratt, 1974). Weiterhin wurden noch Beziehungen zwischen Gingivahyperplasie und Folatmangel vermutet (Vogel, 1977) , 1970). Dies ist ein Beispiel dafür, daß ein Vitamin, für das eine Minderung der Konzentration gefunden wurde, nicht ohne weiteres zusätzlich zu den Antiepileptika substituiert werden kann.…”

Section: Folatunclassified

Nebenwirkungen von Antiepileptika bei Langzeitmedikation

Krause

1988

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“…Even though there have been several research and studies conducted regarding phenytoin-induced enlargement, the key pathogenesis behind the hyperplastic change in the gingival still remain clueless. Literature shows that there is a huge possibility which leads to the gingival changes such as multiple anti-epileptic therapies, plaque deposition, host genetic factors, and reduced serum folate levels [5]. The general agreement would be that, gingival hyperplasia is seen in patients under pheytoin is mainly the consequence of the increase in amount of connective tissue rather than a marked epithelial hyperplasia [6][7].…”

Section: Introductionmentioning

confidence: 98%